Proliferative vitreoretinopathy

Introduction to proliferative vitreoretinopathy Proliferative vitreoretinopathy (PVR) is the main reason for the failure of rhegmatogenous retinal detachment surgery. The pathogenesis of the retinal surface and the vitreous is that the extensive fibroproliferative membrane contracts and pulls to cause retinal detachment. Pigment epithelial cells, glial cells, fibroblasts, fibroblasts and macrophages. Pigment epithelial cells play an important role in the development and progression of proliferative vitreoretinopathy. It is not only the main cell for proliferating membrane formation and contraction. And can produce a catabolic factor that attracts fibroblasts and fibroblasts to participate in the formation of a proliferating membrane. Proliferative vitreoretinopathy has also been called extensive vitreous retraction (MVR), extensive retinal anterior retraction (MPR), and extensive retinal proliferation (MPP). The understanding of PVR has been more than 100 years old. basic knowledge The proportion of illness: 0.002% Susceptible people: no specific population Mode of infection: non-infectious Complications: retinal detachment

Causes of proliferative vitreoretinopathy

Pathology (30%):

The basic pathophysiological processes of PVR are cell proliferation and membrane contraction. Both clinical risk factors and experimental studies are related to two pathological conditions. One is that there is a certain number of cell sources; the other is that there is a stimulating cell proliferation. Factors, retinal tear formation, especially large holes, RPE cells exposed large area; cells are easily activated, strong growth ability; a variety of factors cause blood-retinal barrier destruction, plasma factor exudation, promote cell migration, proliferation and Membrane formation; extracellular matrix such as collagen and fibronectin, the membrane has a stable scaffold, adheres to the retina, causing a fixed scar, becoming the end stage of PVR.

Retinal detachment (30%):

PVR is a common complication of rhegmatogenous retinal detachment (RRD), and it is also one of the main reasons for the failure of RRD surgery and postoperative visual recovery. It is believed that the formation of PVR is a tissue trauma repair process. In the category of scar formation, the most common cause of macular degeneration is tissue hyperplasia in the macula, forming the preretinal membrane, the so-called macular pucker, the proliferation and contraction of the retinal surface cells is the formation of macular folds. The basic pathological process can be roughly divided into three stages:

1 The cells are free and accumulated. When the retina is ruptured, the retinal pigment epithelial cells are free from the vitreous cavity under the stimulation of inflammatory factors, and adhere to the vitreous fibers or the surface of the retina.

2 Cell proliferation and membrane formation, a large number of aggregated retinal pigment epithelial cells begin to proliferate under the stimulation of certain cytokines, phenotypic transformation (which can be transformed into macrophages, fibroblast-like cells), secretion of collagen and various cell activities The substance, together with retinal glial cells, forms a cellular membrane on the vitreous, retina and macular surface.

3 The formation and contraction of the vitreous retinal proliferative membrane, traction of the retina and the macula (vertical or tangential traction), the formation of typical proliferative vitreoretinopathy and traction retinal or macular detachment, and for some reasons (such as long-term supine position) These proliferating cells adhere to the macular area or the macular for a long time, and form a dense cellular membrane under the macula and the macula - the macular epiretinal membrane and the macular epithelium. Due to the presence and contraction of the membrane, Lead to macular edema, cone cell malnutrition, degeneration and necrosis and other changes, visual acuity decreased seriously.

Eye penetrating injury (30%):

The traumatic proliferative vitreoretinopathy caused by traumatic macular retinal lesions, the pathophysiological process is also an over-repairing response of the eye tissue to the wound, but because of the different causes, the cells on the surface of the vitreous or retinal macula There are slight differences in composition and type. In traumatic macular wrinkles, due to the presence of inflammatory reactions and vitreous hemorrhage, cell proliferation is dominated by macrophages and fibroblasts, and retinal pigment epithelial cells and glial cells are Auxiliary (referring to those without retinal tears), so the formation of the macular anterior membrane is thick and tough, and the damage to the macular tissue is more serious.

Proliferative vitreoretinopathy prevention

Eat properly according to the doctor's advice. Visual symptoms have blurred vision, one eye or two eyes suddenly have decreased vision, and there are black spots or flashes in the field of vision. All eyes should be consulted by an ophthalmologist at all times, paying attention to eye hygiene: avoiding close-up eyes and staying close to the eye. Excessive smoking cessation; smoking can cause accelerated retinopathy. There is no effective preventive measure for this disease. Early detection and early diagnosis are the key to the prevention and treatment of this disease.

Proliferative vitreoretinopathy complications Complications

Retinal detachment is the most common and most serious complication of PVR.

Symptomatic symptoms of proliferative vitreoretinopathy Common symptoms Visually deformed visually small

1. The presence of brown particles and gray cell clusters in the vitreous is the expression of RPE cell release and proliferation. The soot-like particles indicate that the cells contain pigments, and the melanin particles in the RPE cells are diluted by multiple division and proliferation in the vitreous, and the pigment is reduced. Therefore, the presence of pigment particles indicates that the cells have not begun to proliferate significantly; and the appearance of gray cell clusters in the vitreous is an early clinical manifestation of cell proliferation.

2. When RPE cells begin to proliferate, vitreous opacity increases and there are protein streaks, suggesting that blood-eye barrier damage leads to plasma exudation.

3. Retinal stiffness and wrinkles appear, which is the expression of proliferative membrane formation and contraction. In the location of the hole, even if the membrane is not visible, the edge of the slit or the cover film is pulled toward the base of the vitreous, indicating the presence of the membrane. As the disease progresses, the detached retina changes from movable to stiff; the proliferative membrane forms on the anterior and posterior surface of the retina and in the vitreous, causing irregular wrinkles in the retina, distort or straighten blood vessels, star wrinkles, diffuse wrinkles, and annular contractions. form.

4. The posterior membrane of the retina is common in PVR. According to statistics, it accounts for 47% of the cases. Most of them (72%) do not affect the effect of retinal reattachment surgery. The visual prognosis is still good; but 28% must be surgically treated. Clinically, the retina The posterior membrane has a variety of appearances, such as lines, dendrites, nets, rings or tubular strips, which can be layered, into a piece of tissue, can be pigmented, or grayish yellow, because such membranes are mainly composed of The retinal pigment epithelial cells are composed of tubular, centrally surrounded by collagen strips that can be completely removed during surgery.

5. Pulling retinal detachment When the posterior retina is completely creased, a typical funnel-like detachment is formed when the posterior vitreous plane is contracted, and the retina of the peripheral retina is pulled back and forth to form a narrow funnel.

The progression of the above course may be stable at any stage, or may develop slowly within a few months, but some cases may develop into a funnel-shaped detachment within a few hours. After one operation, some observations indicate that the case of retinal detachment is diagnosed as PVR. The average time is 4 weeks, but it can be as long as 1 year; however, in 6 months or more, the chance of PVR is very low after retinal surgery.

6. The 1991 classification includes a detailed description of the posterior and anterior PVR contractions and is divided into 5 types: limited, diffuse, subretinal, annular, and anterior with retinal forward displacement, for PVR The degree is more accurately determined, not only divided into 1 to 4 quadrants, but divided into 1 to 12 hours. Compared with the 1983 classification, A and B are the same, and C and D are combined to C. The C level is subdivided into CP (rear) and CA (front), and the original D level is not used.

(1) Rear PVR:

1 Local contraction, that is, 1 or several isolated contraction centers (star wrinkles), usually have little effect on the entire detachment pattern.

2 diffuse contraction, refers to the irregular retinal folds that fuse with each other, making the posterior retina a funnel shape, the wrinkles radiating forward to the serrated edge, and the optic disc may not be visible.
3 subretinal contraction, formed by the posterior retinal membrane of the annular narrowing around the optic disc (napkin ring), or a line of wrinkles (clothing line), mainly ring traction.

(2) Front PVR:

1 annular contraction, caused by the anterior membrane of the equator to cause irregular folds of the anterior retina, the retina contracted in the circumferential direction, so that the posterior portion formed radial folds, while the retina of the base of the vitreous body pulled inward.

2 anterior contraction, caused by contraction of the proliferative membrane along the posterior vitreous surface, the direction of the force is perpendicular to the surface of the retina; or in the eye that has undergone vitrectomy or perforation, the proliferative membrane is found in the anterior vitreous, the residual posterior vitreous or vitreous base surface The traction is mainly in the anterior-posterior direction, and the detached retina is pulled forward. The foremost retina forms a basin shape, which may have abnormal adhesion, and adhesion to the ciliary process may form low intraocular pressure, and adhesion with the iris may cause the iris to contract backward. .

Examination of proliferative vitreoretinopathy

Auxiliary inspection

(1) fundus fluorescein angiography: due to retinal blood vessels being pulled by the fibrous membrane, fluorescein angiography can show retinal vein variability, filling delay, small blood vessels around the macula, and gathering, sometimes visible small fluorescein leakage points, such as the macular area Extensive exudation, diffuse or cystic edema, can be seen in a wide range of fluorescein leakage points, sometimes fused together in a petal shape, sometimes in the form of large patches of strong fluorescence.

(2) OCT: In the macular lesions caused by PVR, OCT examination has many different manifestations: vitreous macular traction; irregular macular anterior membrane; macular retinal neuroepithelial edema, thickening, cystic or detachment; sometimes visible Micro wrinkles of the retinal pigment epithelium.

(3) Multifocal electroretinogram (mERG): There is not much difference between mURG-induced macular degeneration caused by PVR and other causes of macular degeneration. The mERG three-dimensional topographic map shows that the macular peaks are significantly reduced or disappeared, or in spikes. The surrounding has a wavy appearance; the mERG graph shows a wave, and the b-wave amplitude is also significantly reduced.

2. Auxiliary examination and evaluation of macular function in refractive interstitial opacity: In the case of turbidity of glass body weight, it is very difficult to accurately determine the condition of the macula and evaluate the function of the macula. At this time, necessary examinations such as light perception, light localization examination and B-ultrasound The examination is particularly important. B-ultrasound can not only understand the distribution and activity of the vitreous fiber membrane, but also show the retinal and macular area of the posterior pole more clearly. In the macular lesion caused by PVR, the B-ultrasound can show the posterior pole. The echo in the retina and macular area is enhanced, and the macular traction strip, the macular anterior membrane, the presence or absence of macular detachment, and the understanding of posterior vitreous detachment can be found.

Diagnosis and differentiation of proliferative vitreoretinopathy

According to the patient's clinical manifestations and fundus conditions, combined with B-ultrasound and fundus fluorescein angiography results, can be diagnosed.

Generally not confused with other diseases.

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